Foam rolling is thought to improve muscular function, performance, overuse, and joint range of motion (ROM); however, there is no empirical evidence demonstrating this. Thus, the objective of the study was to determine the effect of self-myofascial release (SMR) via foam roller application on knee extensor force and activation and knee joint ROM. Eleven healthy male (height 178.9 ± 3.5 cm, mass 86.3 ± 7.4 kg, age 22.3 ± 3.8 years) subjects who were physically active participated. Subjects' quadriceps maximum voluntary contraction force, evoked force and activation, and knee joint ROM were measured before, 2 minutes, and 10 minutes after 2 conditions: (a) 2, 1-minute trials of SMR of the quadriceps via a foam roller and (b) no SMR (Control). A 2-way analysis of variance (condition × time) with repeated measures was performed on all dependent variables recorded in the precondition and postcondition tests. There were no significant differences between conditions for any of the neuromuscular dependent variables. However, after foam rolling, subjects' ROM significantly (p < 0.001) increased by 10° and 8° at 2 and 10 minutes, respectively. There was a significant (p < 0.01) negative correlation between subjects' force and ROM before foam rolling, which no longer existed after foam rolling. In conclusion, an acute bout of SMR of the quadriceps was an effective treatment to acutely enhance knee joint ROM without a concomitant deficit in muscle performance.

The most important findings of the present study were that FR was beneficial in attenuating muscle soreness while improving vertical jump height, muscle activation, and passive and dynamic ROM in comparison with control. FR negatively affected several evoked contractile properties of the muscle, except for half relaxation time and EMD, indicating that FR benefits are primarily accrued through neural responses and connective tissue.

Inflammation can arise in response to a variety of stimuli, including infectious agents, tissue injury, autoimmune diseases, and obesity. Some of these responses are acute and resolve, while others become chronic and exert a sustained impact on the host, systemically, or locally. Obesity is now recognized as a chronic low-grade, systemic inflammatory state that predisposes to other chronic conditions including metabolic syndrome (MetS). Although obesity has received considerable attention regarding its pathophysiological link to chronic cardiovascular conditions and type 2 diabetes, the musculoskeletal (MSK) complications (i.e., muscle, bone, tendon, and joints) that result from obesity-associated metabolic disturbances are less frequently interrogated. As musculoskeletal diseases can lead to the worsening of MetS, this underscores the imminent need to understand the cause and effect relations between the two, and the convergence between inflammatory pathways that contribute to MSK damage. Muscle mass is a key predictor of longevity in older adults, and obesity-induced sarcopenia is a significant risk factor for adverse health outcomes. Muscle is highly plastic, undergoes regular remodeling, and is responsible for the majority of total body glucose utilization, which when impaired leads to insulin resistance. Furthermore, impaired muscle integrity, defined as persistent muscle loss, intramuscular lipid accumulation, or connective tissue deposition, is a hallmark of metabolic dysfunction. In fact, many common inflammatory pathways have been implicated in the pathogenesis of the interrelated tissues of the musculoskeletal system (e.g., tendinopathy, osteoporosis, and osteoarthritis). Despite these similarities, these diseases are rarely evaluated in a comprehensive manner. The aim of this review is to summarize the common pathways that lead to musculoskeletal damage and disease that result from and contribute to MetS. We propose the overarching hypothesis that there is a central role for muscle damage with chronic exposure to an obesity-inducing diet. The inflammatory consequence of diet and muscle dysregulation can result in dysregulated tissue repair and an imbalance toward negative adaptation, resulting in regulatory failure and other musculoskeletal tissue damage. The commonalities support the conclusion that musculoskeletal pathology with MetS should be evaluated in a comprehensive and integrated manner to understand risk for other MSK-related conditions. Implications for conservative management strategies to regulate MetS are discussed, as are future research opportunities.

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Childhood obesity is a major risk factor for heart disease during adulthood, independent of adulthood behaviours. Therefore, it seems that childhood obesity leads to partly irreversible decrements in cardiac function. Little is known about how obesity during maturation affects the mechanical properties of the heart. The purpose of this study was to evaluate contractile properties in developing hearts from animals with dietary-induced obesity (high-fat high-sucrose diet (HFHS)). We hypothesized that obesity induced during adolescence results in decrements in cardiac contractile function. Three-week old rats (n=16) were randomized into control (chow) or dietary-induced obesity (HFHS) groups. Following 14 weeks on the diet, skinned cardiac trabeculae fibre bundle testing was performed to evaluate active and passive force, maximum shortening velocity, and calcium sensitivity. Rats in the HFHS group had significantly larger body mass and total body fat percentage. There were no differences in maximal active or passive properties of hearts between groups. Hearts from HFHS group rats had significantly slower maximum shortening and lower calcium sensitivity than controls. Decreased shortening velocity and calcium sensitivity in hearts of obese animals may constitute increased risk of cardiac disease in adulthood. Novelty Bullets • Cardiac muscle from animals exposed to an obesogenic diet during development had lower shortening velocity and calcium sensitivity than those from animals fed a chow diet. • These alterations in mechanical function may be a mechanism for the increased risk of cardiac disease observed in adulthood.